title: Enhanced pathogenicity of biofilm-negative Staphylococcus epidermidis isolated from platelet preparations.
abstract: BACKGROUND
  The platelet (PLT) storage environment triggers the formation of surface-attached aggregates known as biofilms by the common PLT contaminant Staphylococcus epidermidis. The biofilm matrix is largely composed of polysaccharide intercellular adhesin (PIA) mediated by the icaADBC operon. However, PIA-negative S. epidermidis has been reported to form biofilms in PLT concentrates (PCs). Since biofilm formation is associated with increased virulence, this study was aimed at determining if PIA-negative S. epidermidis grown in PCs presents enhanced virulence using the nematode Caenorhabditis elegans as a host model for bacterial pathogenesis.
  
  
  METHODS
  Biofilm-positive S. epidermidis ATCC 35984 and 9142, which carry the icaADBC operon, and biofilm-negative S. epidermidis ATCC 12228 and 9142 ΔicaA were grown in regular media and in PCs and biofilm formation was quantified using a crystal violet assay. The virulence of these strains after passage through PCs was tested using nematode killing assays. Nematode survival was calculated using the Kaplan-Meier method and statistical differences were determined by log-rank analysis.
  
  
  RESULTS
  All S. epidermidis strains were able to form biofilms in PCs. Although persistence of a biofilm-positive phenotype in the biofilm-negative strains grown in PCs was not observed after passage in regular medium, the virulence of all strains was significantly increased as demonstrated by shortened life spans of the nematodes in C. elegans killing assays.
  
  
  CONCLUSIONS
  Our findings highlight the potential of an increased risk of nosocomial infections caused by S. epidermidis in transfusion recipients since PC storage conditions promote biofilm formation, and possibly pathogenicity, of strains traditionally known to be attenuated for virulence.
authors.affiliation: Department of Microbiology, Faculty of Science, University of Manitoba, Winnipeg, Manitoba, Canada; Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia; Canadian Blood Services, Ottawa, Ontario, Canada.
authors.forename: Scott D
authors.initials: SD
authors.lastname: Hodgson
authors.forename: Valerie
authors.initials: V
authors.lastname: Greco-Stewart
authors.forename: Celine S
authors.initials: CS
authors.lastname: Jimenez
authors.forename: Costi D
authors.initials: CD
authors.lastname: Sifri
authors.forename: Ann Karen C
authors.initials: AK
authors.lastname: Brassinga
authors.forename: Sandra
authors.initials: S
authors.lastname: Ramirez-Arcos
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics; D018441:Biofilms / Q000254:growth & development*; D001681:Biological Assay / Q000379:methods; D001792:Blood Platelets / Q000382:microbiology*; D017173:Caenorhabditis elegans / Q000382:microbiology*; D017353:Gene Deletion; D006801:Humans; D017713:Platelet Transfusion / Q000592:standards*; D011135:Polysaccharides, Bacterial / Q000378:metabolism; D013203:Staphylococcal Infections / Q000097:blood* / Q000517:prevention & control; D013212:Staphylococcus epidermidis / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D014774:Virulence
chemical_list: D001426:Bacterial Proteins; D011135:Polysaccharides, Bacterial; C113579:polysaccharide intercellular adhesin